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Melons-gaston.com

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Conversion Technology Metas Server
Melons-gaston.com is hosted in Italy . Melons-gaston.com doesn't use HTTPS protocol. Number of used technologies: 1. First technologies: Html, Number of used javascripts: 0. Number of used analytics tools: 0. Its server type is: Apache.

Technologies in use by Melons-gaston.com

Technology

Number of occurences: 1
  • Html

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Server Type

  • Apache

Conversion rate optimization
visitors Clickable call number Not founded!
visitors Conversion form (contact form, subcriber) Not founded!
visitors Clickable email Not founded!
visitors CTA (call to action) button Not founded!
visitors List Not founded!
visitors Image Not founded!
visitors Enhancement Not founded!
visitors Responsive website Not founded!
visitors Facebook sharing Not founded!
visitors Google+ sharing Not founded!
visitors Twitter sharing Not founded!
visitors Linkedin sharing Not founded!
visitors Blog on the webiste Not founded!

HTTPS (SSL) - Melons-gaston.com

Missing HTTPS protocol.

    Meta - Melons-gaston.com

    Number of occurences: 0

    Server / Hosting

    • IP: 81.88.57.68
    • Latitude: 43.15
    • Longitude: 12.11
    • Country: Italy

    Rname

    • ns2.amenworld.com
    • ns1.amenworld.com
    • mail-fr.securemail.pro

    Target

    • root.amen.fr

    HTTP Header Response

    HTTP/1.1 200 OK Date: Fri, 22 Jul 2016 12:12:05 GMT Server: Apache Vary: Host Last-Modified: Tue, 12 Feb 2013 19:23:30 GMT Accept-Ranges: bytes Content-Length: 99 Content-Type: text/html Content-Language: fr X-Cache: MISS from s_hp65 X-Cache-Lookup: MISS from s_hp65:80 Via: 1.1 s_hp65 (squid/3.5.19) Connection: keep-alive

    DNS

    host: melons-gaston.com
    1. class: IN
    2. ttl: 900
    3. type: A
    4. ip: 81.88.57.68
    host: melons-gaston.com
    1. class: IN
    2. ttl: 900
    3. type: NS
    4. target: ns2.amenworld.com
    host: melons-gaston.com
    1. class: IN
    2. ttl: 900
    3. type: NS
    4. target: ns1.amenworld.com
    host: melons-gaston.com
    1. class: IN
    2. ttl: 900
    3. type: SOA
    4. mname: ns1.amenworld.com
    5. rname: root.amen.fr
    6. serial: 2013021201
    7. refresh: 86400
    8. retry: 7200
    9. expire: 2592000
    10. minimum-ttl: 300
    host: melons-gaston.com
    1. class: IN
    2. ttl: 900
    3. type: MX
    4. pri: 10
    5. target: mail-fr.securemail.pro

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    This list shows You some spelling mistakes at internet search for this domain.

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      712 North • NOBODY WANTS TO GO BLIND. • Novel small molecules that effectively inhibit a mitochondrial metalloprotease critical for retinal ganglion cells provide a new method for therapeutic intervention in glaucoma, the leading cause of incurable blindness. • Strategic positioning targeting dominant optic atrophy, an orphan disease related to glaucoma. The Problem: Glaucoma – the leading cause of incurable blindness – is a progressive optic neuropathy that leads to irreversible loss of retinal ganglion cells causing diminished visual function and blindness. To date, there are no available therapies that directly target retinal ganglion cells. Instead, all current treatments focus on lowering intraocular pressure, a major risk factor for glaucoma, and only an estimated 30% of patients respond to those therapies. Thus, due to its high incidence, complex etiology, and lack of available therapies, there is an unmet need for neuroprotective drugs to treat glaucoma. The Solution: We are developing neuroprotective drugs to treat glaucoma by targeting the mitochondrial quality control pathway. To this end we are screening for small molecules to identify compounds that can prevent retinal ganglion cell loss. We are initially focusing on dominant optic atrophy, an orphan optic neuropathy with a shared mechanism-of-action, as our fast-to-market solution. In the long term, our therapeutic approach has significant potential to be highly effective in treating other diseases broadly classified as glaucoma. We will bring an innovative solution to a market that hasn’t seen any new approaches to treatment in decades. Market Opportunity: 1 in 30 adults over 40 years have glaucoma, which equates to 64 million people worldwide with 8.4 million being bilaterally blind. In 2013 there were 3.3 million glaucoma patients in the United States, 6.8 million patients in Europe, and 39 million affected individuals in Asia. With an aging population, these numbers are expected to increase to 76 million people worldwide by 2020 and 112 million people by 2040. Dominant optic atrophy is a juvenile optic neuropathy with a minimum prevalence of 1 in 25,000 people with about 12,000 affected people in the United States and 30,000 individuals in Europe. Estimates predict that >50% of patients carry mutations in the Optic Atrophy 1 (OPA1) gene and nearly 20% developed a more severe neuromuscular phenotype. The glaucoma market currently reaches $2.4 billion in the major markets United States, Europe and Japan and is expected to hit $3.0 billion by 2023. Novel classes of intraocular pressure lowering drugs will mainly drive the growth of the glaucoma market, while there are no treatment options available for patients with dominant optic atrophy. The annual treatment costs for a conventional intraocular pressure lowering therapy can range between $150 and $1,200. Neuroprotective therapies can complement intraocular pressure lowering therapies and we estimate the serviceable obtainable market at $600M to $800M. Our strategic positioning to target an orphan optic neuropathy will speed up market entry and allow us to build our reputation as an innovator in ophthalmology and prepare for commercialization for the larger glaucoma market. We estimate the serviceable obtainable market for dominant optic atrophy at $240M to $280M. Competitive Landscape: Several different neuroprotective glaucoma therapies are currently in development, validating this approach to tackling glaucoma. Calcium antagonists have finished phase II trials (Santen) and showed 10% retinal ganglion cell rescue in preclinical studies. Safety trials investigating CNTF as a neuroprotectant for glaucoma have been completed (Neurotech). CNTF showed some protective effects with 15% greater retinal ganglion cell survival after axotomy in preclinical studies. Genetic knockdown of DLK showed 75% retinal ganglion cell rescue upon optic nerve crush and DLK inhibitors are currently being developed (Genentech; Graybug). Alternative approaches are seeking to replace retinal ganglion cells by adoptive cell therapies. Due to the complexity of the disease, we believe there is room for multiple neuroprotective modalities and our approach will most likely complement existing therapies. There are no treatment options for dominant optic atrophy and the pipeline of drugs in development is limited. Preclinical trials with Idebenone (Santhera) showing efficacy in a small sample of patients remain anecdotal and failed to reproduce in animal studies. Also, a damaging effect for healthy retinal ganglion cells was reported. Other ubiquinone analogues (EPI-743, Edison Pharmaceuticals) are under consideration but no studies have been published so far. Even if these therapies successfully enter the market, significant opportunity remains for a superior, functionally distinct therapeutic with orphan drug status to disrupt and take command of the market. The Model: Our goal is to build a sustainable business advancing therapies for eye diseases. We will generate revenue in two ways: product sales and revenue earned through collaboration arrangements. At this stage we are focused on product development by generating a novel therapy for dominant optic atrophy and establishing a drug-development and preclinical testing platform for neurodegenerative diseases. Growth and de-risking strategies include expanding our pipeline of investigational product candidates for dominant optic atrophy, glaucoma and other neurodegenerative diseases and contract research with strategic partners. The Team: We have built a strong team of clinicians, scientists and entrepreneurs (all UCSF Alumni) to make this venture a success. Marcel V. 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We will also explore the potential for accelerated approval and/or breakthrough status with the FDA. Clinical Development: Glaucoma presents with increasing visual difficulties usually later in life, while dominant optic atrophy classically presents with early childhood onset. Glaucoma is a complex disease with a variety of contributing factors posing challenges in clinical trial design. OPA1 mutations have a high penetrance rate, but the disease is characterized by marked intra- and interfamilial variability. Clinically relevant endpoints for both diseases are structural measurements of the optic disc topography and retinal nerve fiber layer, and visual field changes as measured by standard automated perimetry. The use of these endpoints in clinical trials is potentially limited by the need for large samples, long-term follow-up, and variability of results. 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